The inflammatory response.

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Presentation transcript:

The inflammatory response. The inflammatory response. This simplified overview shows the course of the inflammatory response. An insult triggers the release of PAMPs (pathogen-associated molecular patterns) and/or DAMPs (danger-associated molecular patterns), which are sensed by pattern recognition mechanisms such as receptors (pattern recognition receptors (PRRs) on the cell surface or within the cytosol or nucleus of sensor cells as well as by pattern-recognizing complex systems such as the complement system and others. Therefore, sensors can be different types of cells, tissues/organs, or proteins/other molecules, which themselves may function as effectors to modulate the immune response through various different pro- or anti-inflammatory mediators or biomarkers. As a result, the underlying insult can be cleared or not, and organ function may be temporarily or permanently impaired. LPS, lipopolysaccharide (part of the membrane of Gram-negative bacteria); LTA, lipoteichoic acid (part of the cell wall of Gram-positive bacteria); HMGB1, high-mobility-group protein B1; C5a and C3a, complement components 5a and 3a; C5aR, C5a receptor protein; C5b-9, terminal complement complex; aPPT, activated partial thromboplastin time; PT, prothrombin time; AT, antithrombin; ELAM-1, endothelial leukocyte adhesion molecule 1; ICAM-1, intercellular adhesion molecule 1; CRP, C-reactive protein; LBP, LPS-binding protein; PCT, procalcitonin; IL-6, interleukin-6; MIF, macrophage migration inhibitory factor; sTNF, soluble tumor necrosis factor; suPAR, soluble urokinase-type plasminogen activator receptor; sTREM-1, soluble triggering receptor expressed on myeloid cells 1; mHLA-DR, monocytic human leukocyte antigen DR; CD64 and CD48, integral membrane glycoproteins; DIC, disseminated intravascular coagulation. Konrad Reinhart et al. Clin. Microbiol. Rev. 2012; doi:10.1128/CMR.00016-12